Establishment and characterization of 6 novel patient-derived primary pancreatic ductal adenocarcinoma cell lines from Korean pancreatic cancer patients

The role of microRNA-132 in human pancreatic ductal adenocarcinomas is still ambiguous. We explored the association between microRNA-132 and pancreatic ductal adenocarcinoma prognosis. The expression of microRNA-132 in 50 pancreatic ductal adenocarcinoma tissue samples and pancreatic ductal adenocarcinoma cell lines was examined, and the association between its expression and pancreatic ductal adenocarcinoma prognosis was assessed. Functional analysis and factors downstream of microRNA-132 were investigated. Kaplan-Meier survival curves showed that high expression of microRNA-132 was a significant prognostic factor for 1-year survival of patients with pancreatic ductal adenocarcinoma ( P = .028). Multivariate analysis for overall survival indicated that high expression of microRNA-132 was an independent prognostic factor for patients with pancreatic ductal adenocarcinoma ( P = .044). Low expression of microRNA-132 was associated with poor prognosis in pancreatic ductal adenocarcinoma. Ectopic expression of microRNA-132 significantly inhibited proliferation and promoted apoptosis of 2 pancreatic ductal adenocarcinoma cell lines. Bioinformatic analysis revealed that microRNA-132 may exert its effects on pancreatic ductal adenocarcinoma through downregulating mitogen-activated protein kinase 3 and nuclear transcription factor Y subunit α. The results of this study further our understanding of the relationship between microRNA-132 and pancreatic ductal adenocarcinoma by showing that microRNA-132 might inhibit the progression of pancreatic ductal adenocarcinoma by regulating mitogen-activated protein kinase and nuclear transcription factor Y subunit alpha.

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Omics Approaches in Pancreatic Adenocarcinoma

Cancers ◽

10.3390/cancers11081052 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1052

Author(s):

Iranzu González-Boja ◽

Antonio Viúdez ◽

Saioa Goñi ◽

Enrique Santamaria ◽

Estefania Carrasco-García ◽

...

Keyword(s):

Pancreatic Cancer ◽

Survival Rate ◽

Pancreatic Ductal Adenocarcinoma ◽

Ductal Adenocarcinoma ◽

Curative Intent ◽

Pancreatic Cancers ◽

Wide Range ◽

Prevention And Treatment ◽

Shed Light

Pancreatic ductal adenocarcinoma, which represents 80% of pancreatic cancers, is mainly diagnosed when treatment with curative intent is not possible. Consequently, the overall five-year survival rate is extremely dismal—around 5% to 7%. In addition, pancreatic cancer is expected to become the second leading cause of cancer-related death by 2030. Therefore, advances in screening, prevention and treatment are urgently needed. Fortunately, a wide range of approaches could help shed light in this area. Beyond the use of cytological or histological samples focusing in diagnosis, a plethora of new approaches are currently being used for a deeper characterization of pancreatic ductal adenocarcinoma, including genetic, epigenetic, and/or proteo-transcriptomic techniques. Accordingly, the development of new analytical technologies using body fluids (blood, bile, urine, etc.) to analyze tumor derived molecules has become a priority in pancreatic ductal adenocarcinoma due to the hard accessibility to tumor samples. These types of technologies will lead us to improve the outcome of pancreatic ductal adenocarcinoma patients.

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Pancreatic ductal adenocarcinoma cell lines display a plastic ability to bi-directionally convert into cancer stem cells

International Journal of Oncology ◽

10.3892/ijo.2014.2796 ◽

2014 ◽

Vol 46 (3) ◽

pp. 1099-1108 ◽

Cited By ~ 22

Author(s):

ELISA DALLA POZZA ◽

ILARIA DANDO ◽

GIULIA BIONDANI ◽

JESSICA BRANDI ◽

CHIARA COSTANZO ◽

...

Keyword(s):

Stem Cells ◽

Cancer Stem Cells ◽

Pancreatic Ductal Adenocarcinoma ◽

Cell Lines ◽

Ductal Adenocarcinoma ◽

Adenocarcinoma Cell

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Nestin regulates epithelial-mesenchymal transition marker expression in pancreatic ductal adenocarcinoma cell lines

Molecular and Clinical Oncology ◽

10.3892/mco.2012.1 ◽

2012 ◽

Vol 1 (1) ◽

pp. 83-87 ◽

Cited By ~ 6

Author(s):

MASAHITO HAGIO ◽

YOKO MATSUDA ◽

TAEKO SUZUKI ◽

TOSHIYUKI ISHIWATA

Keyword(s):

Pancreatic Ductal Adenocarcinoma ◽

Cell Lines ◽

Epithelial Mesenchymal Transition ◽

Ductal Adenocarcinoma ◽

Mesenchymal Transition ◽

Adenocarcinoma Cell ◽

Marker Expression

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Oncolytic Activity of Avian Influenza Virus in Human Pancreatic Ductal Adenocarcinoma Cell Lines

Journal of Virology ◽

10.1128/jvi.00929-14 ◽

2014 ◽

Vol 88 (16) ◽

pp. 9321-9334 ◽

Cited By ~ 10

Author(s):

S. B. Kasloff ◽

M. S. Pizzuto ◽

M. Silic-Benussi ◽

S. Pavone ◽

V. Ciminale ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Pancreatic Ductal Adenocarcinoma ◽

Cell Lines ◽

Ductal Adenocarcinoma ◽

Adenocarcinoma Cell ◽

Oncolytic Activity

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Transcriptional regulation of SLIT2 expression in pancreatic cancer cell lines

10.1101/2020.09.29.319129 ◽

2020 ◽

Author(s):

Brenna A. Rheinheimer ◽

Lukas Vrba ◽

Bernard W Futscher ◽

Ronald L Heimark

Keyword(s):

Pancreatic Cancer ◽

Transcriptional Regulation ◽

Pancreatic Ductal Adenocarcinoma ◽

Cell Lines ◽

Cancer Cell ◽

Pancreatic Cancer Cell ◽

Trichostatin A ◽

Cancer Cell Lines ◽

Ductal Adenocarcinoma ◽

Liver Cancers

AbstractBackgroundSLIT2 has been shown to serve as a tumor suppressor in breast, lung, colon, and liver cancers. Additionally, expression of SLIT2 has been shown to be epigenetically regulated in prostate cancer. Therefore, we sought to determine transcriptional regulation of SLIT2 in pancreatic ductal adenocarcinoma.MethodsRNA expression of SLIT2, SLIT3, and ROBO1 was examined in a panel of pancreatic ductal adenocarcinoma cell lines while protein expression of ROBO1 and SLIT2 was examined in tumor tissue. Methylation of the SLIT2 promoter was determined using Sequenom while histone modifications were queried by chromatin immunoprecipitation. Reexpression of SLIT2 was tested by treatment with 5-aza-2’deoxycytidine and Trichostatin A.ResultsPancreatic cancer cell lines fall into three distinct groups based on SLIT2 and ROBO1 expression. The SLIT2 promoter is methylated in pancreatic ductal adenocarcinoma and SLIT2 expression is dependent on the level of methylation at specific CpG sites. Treatment with 5-aza-2’deoxycytidine (but not Trichostatin A) led to SLIT2 reexpression. The SLIT2 promoter is bivalent in pancreatic ductal adenocarcinoma and histone marks around the transcriptional start site are responsible for transcription.ConclusionsLoss of SLIT2 expression modulated by epigenetic silencing may play a role in pancreatic ductal adenocarcinoma progression.

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